We are analyzing https://link.springer.com/article/10.1007/s00262-010-0968-0.

Title:
2011: the immune hallmarks of cancer | Cancer Immunology, Immunotherapy
Description:
Ten years after the publication of the position paper “The hallmarks of cancer” (Hanahan and Weinberg Cell 100:57–70, 2000), it has become increasingly clear that mutated cells on their way to giving rise to a tumor have also to learn how to thrive in a chronically inflamed microenvironment, evade immune recognition, and suppress immune reactivity. Genetic and molecular definition of these three immune hallmarks of cancer offers the opportunity to learn how to deploy specific countermeasures to reverse the situation in favor of the immune system and, eventually, the patient. This new information could be channeled to address what seem to be the three major hallmarks for the immune control of cancer progression: effective procedures to activate immune reactivity; characterization of not-disposable oncoantigens; and counteraction of immune suppression.
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Keywords {🔍}

cancer, article, google, scholar, pubmed, cas, immune, cells, tumor, cell, vaccines, vaccine, mice, immunol, inflammation, nat, rev, forni, hallmarks, mechanisms, ability, tumors, response, immunity, treg, cavallo, carcinogenesis, growth, vaccination, effective, tumour, risk, clinical, antibodies, progression, oncoantigens, suppression, therapeutic, transgenic, carcinoma, target, antitumor, mammary, res, immunotherapy, giovanni, nanni, lollini, microenvironment, recognition,

Topics {✒️}

anti-her2/neu antibody depends tumor necrosis factor-alpha article download pdf anti-cd25 monoclonal antibody cytokine-driven compensatory proliferation oncogene-coded proteins [26 myeloid-derived suppressor cells low-avidity ctl response t-cell-mediated cytotoxicity induced t-cell responses steroidal anti-inflammatory drugs t-cell-mediated immunity epstein-barr virus vaccine c-erbb-2 transgenic balb/ monoclonal antibody-based immunotherapy oncogene-addicted cell population tumor necrosis factor reveals latent low-avidity cd4+ cd25+ suppressor genetically modified mice chronically inflamed microenvironment haemopoietic colony-stimulating activity genome-wide microarray analysis long-lasting tumor immunity hla-a2 transgenic mice intrinsic inflammatory pathways neu/erbb2 transgenic mice high-dose il-2 compared ifn-gamma signaling determine t-cell responses [80] myeloid immature cells castration-resistant prostate cancer pro-inflammatory cytokines [17] immune/inflammatory cells recruited stable immune defects transforming growth factor anti-tumour therapy epstein–barr virus chronic inflammation plays privacy choices/manage cookies activate immune reactivity inflammatory bowel disease anti-inflammatory drugs t-cell receptor international consensus statement anti-her2 strategies class iii oncoantigens lethal cancer show complement-mediated cytotoxicity cell-mediated immunity

Questions {❓}

As their growth hidden from immune recognition is not enough to allay their obsession with attacks on the part of the immune system, most—all?
Can these three hallmarks lead to the formulation of immune procedures effective in tumor therapy?
Cavallo F, Calogero RA, Forni G (2007) Are oncoantigens suitable targets for anti-tumour therapy?
Lazebnik Y (2010) What are the hallmarks of cancer?

Schema {🗺️}

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         headline:2011: the immune hallmarks of cancer
         description:Ten years after the publication of the position paper “The hallmarks of cancer” (Hanahan and Weinberg Cell 100:57–70, 2000), it has become increasingly clear that mutated cells on their way to giving rise to a tumor have also to learn how to thrive in a chronically inflamed microenvironment, evade immune recognition, and suppress immune reactivity. Genetic and molecular definition of these three immune hallmarks of cancer offers the opportunity to learn how to deploy specific countermeasures to reverse the situation in favor of the immune system and, eventually, the patient. This new information could be channeled to address what seem to be the three major hallmarks for the immune control of cancer progression: effective procedures to activate immune reactivity; characterization of not-disposable oncoantigens; and counteraction of immune suppression.
         datePublished:2011-01-26T00:00:00Z
         dateModified:2011-01-26T00:00:00Z
         pageStart:319
         pageEnd:326
         license:https://creativecommons.org/licenses/by-nc/2.0
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            Inflammation
            Immune surveillance
            Immune suppression
            Oncoantigens
            Tumor vaccine
            Antitumor antibodies
            Oncology
            Immunology
            Cancer Research
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      headline:2011: the immune hallmarks of cancer
      description:Ten years after the publication of the position paper “The hallmarks of cancer” (Hanahan and Weinberg Cell 100:57–70, 2000), it has become increasingly clear that mutated cells on their way to giving rise to a tumor have also to learn how to thrive in a chronically inflamed microenvironment, evade immune recognition, and suppress immune reactivity. Genetic and molecular definition of these three immune hallmarks of cancer offers the opportunity to learn how to deploy specific countermeasures to reverse the situation in favor of the immune system and, eventually, the patient. This new information could be channeled to address what seem to be the three major hallmarks for the immune control of cancer progression: effective procedures to activate immune reactivity; characterization of not-disposable oncoantigens; and counteraction of immune suppression.
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         Inflammation
         Immune surveillance
         Immune suppression
         Oncoantigens
         Tumor vaccine
         Antitumor antibodies
         Oncology
         Immunology
         Cancer Research
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               type:PostalAddress
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            name:Alma Mater Studiorum University of Bologna, Cancer Research Section
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      name:Department of Clinical and Biological Sciences, University of Turin, Molecular Biotechnology Center, Turin, Italy
      name:Department of Hematology and Oncologic Sciences “L. & A. Seragnoli”, Alma Mater Studiorum University of Bologna, Cancer Research Section, Bologna, Italy

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